CandidaImmunity

Abstract

The human pathogenic fungus Candida albicans is the predominant cause of both superficial and invasive forms of candidiasis. C. albicans primarily infects immunocompromised individuals as a result of either immunodeficiency or intervention therapy, which highlights the importance of host immune defences in preventing fungal infections. The host defence system utilises a vast communication network of cells, proteins, and chemical signals distributed in blood and tissues, which constitute innate and adaptive immunity. Over the last decade the identity of many key molecules mediating host defence against C. albicans has been identified. This review will discuss how the host recognises this fungus, the events induced by fungal cells, and the host innate and adaptive immune defences that ultimately resolve C. albicans infections during health.

Immunity to Candida Infection: An Overview

“…Activation of C5 triggers the formation of C5b, which facilitates the phagocytosis and release of terminal complement components [14]. Binding of Candida surface proteins like Gpm1, Pra 1 and Gpd2 prevents recognition and phagocytosis [15]. Deficiency of complement leads to poor host resistance against candidiasis.…”

“…Among various mechanisms responsible for PMN mediated killing of Candida spp., the 'oxidative burst' appears to be the most prominent. Oxidative burst is the process of rapid formation of reactive oxygen intermediates [14,15]. This process requires assembly of the NADPH oxidase enzyme complex in the cytoplasmic or phagosomal membrane to release superoxide [14,15].…”

“…Oxidative burst is the process of rapid formation of reactive oxygen intermediates [14,15]. This process requires assembly of the NADPH oxidase enzyme complex in the cytoplasmic or phagosomal membrane to release superoxide [14,15]. Natural killer (NK) cell system is another important innate host defence mechanism against candidiasis.…”

“…Studies of various researchers have documented protective role of IL-17 in mucocutaneous and disseminated candidiasis. IL-17 is known to reduce fungal load [15].…”

“…IL-22 plays a vital role in restricting the growth of fungus and maintaining epithelial barrier function. The polymorphisms in the IL-22 gene associated with protection against RVVC can be correlated with elevated IL-22 level and decreased levels of IL-17 and TNFα [15].…”